A number of other therapies for CIN have been investigated, including the following:
- Sodium bicarbonate
- N-acetylcysteine (NAC)
- Statins
- Ascorbic acid [ 31]
- The adenosine antagonists theophylline and aminophylline
- Vasodilators
- Forced diuresis
- Renal replacement therapy
What are the treatment options for contrast-induced nephropathy?
Contrast-Induced Nephropathy Treatment & Management 1 Approach Considerations. Prevention is the cornerstone of contrast-induced nephropathy (CIN)... 2 Hydration Therapy. The first study revealing the benefit of hydration in CIN prevention came... 3 Statins. Statins are widely used in coronary artery disease (CAD) for their pleiotropic effects...
What is contrast-induced nephropathy (CIN)?
Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases.
What is the role of statins in the treatment of contrast-induced nephropathy?
Statins for prevention of contrast-induced nephropathy in patients undergoing non-emergent percutaneous coronary intervention. Nephrology (Carlton) 2010;15:165–70.
How long does contrast cause nephropathy?
Contrast-induced nephropathy most commonly manifests as a nonoliguric and asymptomatic transient decline in renal function [16]. The serum creatinine level begins to rise within 24 hr of contrast administration, usually peaks within 3–5 days, and returns to baseline within 10–14 days [11, 17].
How long does contrast-induced nephropathy last?
CIN is normally a transient process, with renal function reverting to normal within 7-14 days of contrast administration. Less than one-third of patients develop some degree of residual renal impairment.
How do you reduce contrast-induced nephropathy?
Despite extensive study of a variety of agents for renal protection, use of low or isoosmolar contrast agents and IV hydration with normal saline or sodium bicarbonate are the only strategies that have been shown to be effective in the reduction of CIN in those at risk.
Is kidney damage from contrast dye reversible?
The symptoms can be similar to those of kidney disease, which include feeling more tired, poor appetite, swelling in the feet and ankles, puffiness around the eyes, or dry and itchy skin. In many cases, CIN is reversible and people can recover.
What are the drugs that can prevent contrast-induced nephropathy?
Medication Summary Hydration therapy, typically with intravenous isotonic saline, is the cornerstone of contrast-induced nephropathy (CIN) prevention. However, other agents have have demonstrated some benefit in prevention of CIN, including N-acetylcysteine (NAC) and statins.
How do you prevent renal failure with contrast?
These are to 1) prescribe intensive hydration prior to the procedure, 2) reduce the contrast volume injected to a minimum, and 3) use iso- or low-osmolarity contrast agents. Patients at increased risk of CIN include those having previous chronic kidney disease (CKD), especially if diabetes is also present.
Do you need dialysis after contrast?
Unless an unusually large volume of contrast medium is administered, or there is substantial underlying cardiac dysfunction, there is no need for urgent dialysis after intravascular iodinated contrast medium administration [91].
Is Contrast induced nephropathy treatable?
Treatment. There is no definitive treatment available for established CIN; therefore, the benefit for CM-based diagnostic studies or interventional procedures should always be weighed against the risk of CIN. In addition, repeated exposure to CM within a short period of time should be avoided whenever possible.
How long does it take for contrast dye to leave your system?
With normal kidney function, most of the gadolinium is removed from your body in the urine within 24 hours. If you have acute renal failure or severe chronic kidney disease and receive a gadolinium-based contrast agent, there may be a very small risk of developing a rare condition.
How long does it take for contrast to cause AKI?
CI-AKI usually presents within 24 to 48 hours of exposure to iodinated contrast media, with elevation in creatinine and, rarely, oliguria.
What are risk factors for contrast-induced nephropathy?
Non-modifiable risk factors include pre-existent renal insufficiency, diabetes mellitus, older age, reduced left ventricle systolic function, advanced heart failure, acute myocardial infarction, and shock, while volume and type of CM, concomitant use of nephrotoxic medications, hypotension, dehydration, hypoalbuminemia ...
What medication should be held if a patient is receiving contrast dye?
To avoid this complication, metformin must be withheld after the administration of the contrast agent for 48 hours, during which the contrast-induced renal failure becomes clinically apparent. If renal function is normal at 48 hours, the metformin can be restarted.
What GFR is safe for IV contrast?
For CT, eGFR > 45 indicates no increased risk of kidney damage from contrast material. eGFR > 30, but less than 45 indicates that while it is safe to get contrast material, there is a small risk of causing kidney damage.
Can CT scan contrast damage kidneys?
CT contrast materials do rarely cause kidney damage and a skin disorder called nephrogenic systemic fibrosis (NSF) can be caused by the MRI contrast agents. Patients with poor kidney function are the people at risk for these side effects.
Does contrast cause kidney damage?
A very important unwanted effect of the use of contrast drugs is acute kidney injury (AKI), ie, a sudden decrease of renal function due to renal damage. 7 AKI secondary to contrast drugs is called contrast-induced AKI (CI-AKI; or contrast-induced nephropathy [CIN]); it is actually an iatrogenic AKI.
How long do side effects of iodine contrast last?
Patients at increased risk of late skin reactions are those with a history of previous contrast medium reaction and those on interleukin-2 treatment. Most skin reactions are self-limiting and resolve within a week.
How long does gadolinium toxicity last?
With time, symptoms may go away or significantly subside, but patients reported on in our Survey of the Chronic Effects of Retained Gadolinium from Contrast MRIs, have been dealing with their chronic symptoms for up to 5 years with no end in sight.
How long does it take for creatinine to change after contrast exposure?
There is usually a 24-48 h delay between contrast exposure and the change in Scr. This delay makes creatinine a late indicator of renal function changes,[37] therefore more sensitive markers of renal injury are desirable. In fact, several biomarkers of tubular injury have been under evaluation
What is CIN in a nephropathy?
Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.
What is the treatment for CIN?
Treatment of CIN is mainly supportive, consisting of careful fluid and electrolyte management, although dialysis may be required in some cases.[6] The limitation in the available treatment options makes prevention the cornerstone of management.
How long does it take for renal impairment to return to baseline after contrast?
A temporal link is thus implied. Post-contrast exposure, serum creatinine levels peak between two and five days and usually return to baseline in 14 days.
Why is iodine used in contrast media?
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, ...
What is CIN in contrast?
Currently, the understanding of CIN is that it is the impairment of renal function gauged as either a 25% rise in serum creatinine from baseline or an increase of 0.5 mg/dL (44 µmol/L) in absolute serum creatinine value within 48-72 hours following intravenous contrast administration.
What is Contrast-Induced Nephropathy and What Causes It?
Contrast-induced nephropathy (CIN) is a type of kidney disease caused by the dye/contrast that is injected into the blood vessels during various examination procedures such as an angiography. The vast majority of people who under go these procedures and who are injected with this contrast will never develop CIN. However, those with diabetes, previous or current kidney disease, high blood pressure, and those over the age of 75 are all at an increased risk for CIN.
What happens when the kidneys are constricted?
The various vessels in the kidneys are constricted, leading to possible damage and decreased function.
What are the symptoms of kidney failure?
The kidneys function to help the body excrete or eliminate various waste products from the body through urine. Since CIN causes damage and decreased function of the kidneys, the kidneys are not able to adequately excrete these waste products, leading to a build-up of these waste products in the blood. Symptoms that are often associated with the build-up of these waste products in the blood include: 1 Fatigue 2 Nausea and vomiting 3 Weakness 4 Headaches
Does contrast damage kidneys?
It is not completely understood why the contrast damages the kidneys. However, many experts believe that damage may be caused by the following processes:
How long before contrast induced nephropathy?from ncbi.nlm.nih.gov
Patients suffering from contrast-induced nephropathy usually have a preceding history of contrast administration, 24-48 hours before the presentation, while undergoing a diagnostic or therapeutic procedure, such as percutaneous coronary intervention. Acute kidney injury is mostly nonoliguric.
Why do we need a physical exam for nephropathy?from ncbi.nlm.nih.gov
A physical examination is helpful in ruling out other possible causes of acute nephropathies, for instance, cholesterol emboli (pathognomonic findings of which are blue toes and livedo reticularis) or interstitial nephritis secondary to drugs (that typically involves a rash). There may be signs of volume depletion or there could be decompensated heart failure.
What is the third leading cause of iatrogenic acute kidney injury?from ncbi.nlm.nih.gov
Contrast-induced nephropathy is the third leading cause of iatrogenic acute kidney injury. The commonest cause is hypoperfusion of the kidneys causing either prerenal injury or acute tubular necrosis.[10] Moreover, the number and the type of risk factors directly affect the incidence of renal impairment. The incidence rate also depends on the procedure, with reports in the literature varying from 1.6-2.3% for diagnostic investigations to 14.5% overall in coronary intervention. [11]
What is CIN in contrast?from ncbi.nlm.nih.gov
Currently, the understanding of CIN is that it is the impairment of renal function gauged as either a 25% rise in serum creatinine from baseline or an increase of 0.5 mg/dL (44 µmol/L) in absolute serum creatinine value within 48-72 hours following intravenous contrast administration.[1]
Why is iodine used in cardiac procedures?from ncbi.nlm.nih.gov
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, diabetes mellitus, hypertension, and kidney failure due to contrast-induced nephropathy remains a growing concern. A sudden change in kidney function is a common complication of coronary angiography, and percutaneous coronary intervention, primarily because of contrast-induced acute kidney injury or contrast-induced nephropathy. This activity reviews the pathophysiology of contrast-induced nephropathy and highlights the role of the interprofessional team in its management and prevention.
How long does it take for renal impairment to return to baseline after contrast?from ncbi.nlm.nih.gov
A temporal link is thus implied.[2] Post-contrast exposure, serum creatinine levels peak between two and five days and usually return to baseline in 14 days.
How long does it take for creatinine to rise after contrast?from ncbi.nlm.nih.gov
In contrast-induced nephropathy, serum creatinine usually begins to rise within 24 hours after the administration of contrast media, peaks between 3 and 5 days, and comes back to baseline in 7-10 days. A surrogate marker of renal function, serum cystatin C, is increased in patients with contrast-induced nephropathy.
What is ICA induced nephropathy?
ICA-induced nephropathy is the third most common cause of hospital-acquired kidney injury. Overall, the risk of ICA-induced nephropathy is approximately 3%–6%. Several factors can increase the risk of ICA-induced nephropathy ( Box 3) and its occurrence can significantly impact clinical outcomes of a patient in the form of premature mortality and increased health care costs due to prolonged hospital stay. Therefore, several studies have focused on determining patient and contrast factors that can reduce the incidence of ICA-induced nephropathy and these are discussed below.
How long after contrast can you perform hemofiltration?
Hemofiltration (HF) performed 4 to 6 hours before and 18 to 24 hours after contrast reduced the incidence of CIN, in-hospital events, need for acute dialysis, and both in-hospital and 1-year mortality. In contrast, the HF postprocedure alone offered no benefit beyond standard prophylaxis.
What is CIN in contrast?
Contrast-induced nephropathy (CIN), is the development of acute kidney injury after administration of intravascular iodinated contrast. The definition and risk of CIN is poorly understood and remains a contentious subject with controversy regarding the causal relationship between IV contrast and acute kidney injury. There are no prospective randomized controlled trials confirming such an association. Indeed, several large cohort studies based on IV contrast administration for computed tomography have shown no increased risk of acute kidney injury in patients with estimated glomerular filtration rate ≥ 30, and a recent study including data from 5.9 million patients concluded the risk of CIN is ‘‘likely low but likely not zero.’’5,6 Because those with chronic kidney disease may have a higher risk of CIN, it is reasonable to have a baseline renal function established before IV contrast administration. Renal function can be assessed by measuring creatinine and calculating the estimated glomerular filtration rate. Those with chronic kidney disease should be counseled about its risk before receiving contrast. Preventing CIN in these patients centers around optimization of hemodynamic status, usually via intravenous fluids and bicarbonates. 7 Other proposed preventative measures include minimizing volume of contrast, using low or isoosmolar nonionic contrast agents, and administrating the antioxidant N-acetylcysteine.
Is NAC good for CIN?
N-acetylcysteine (NAC) is an antioxidant that is commonly used for CIN prevention. Approximately half of the published randomized controlled trials demonstrate benefit, whereas several metaanalyses suggest either large benefit or no benefit. Beneficial studies are notable for early publication dates, small size, and low quality. Despite the enrollment of nearly 3000 patients, including CKD patients, no beneficial effect of NAC on hard clinical outcomes is noted. The most damning study for NAC as a useful agent to prevent CIN is the Acetylcysteine for Contrast-Induced Nephropathy Trial. This study included 2308 patients and documented no benefit with NAC therapy in the prevention of CIN; the same percentage of NAC- and placebo-treated patients developed CIN (12.7%). Thus, NAC appears to offer no protection against CIN. However, given its favorable safety profile, low cost, easy administration, and wide availability, one could argue for continued use of the drug as prophylaxis. Despite a lack of data, it is reasonable to avoid nonsteroidal antiinflammatory drugs (NSAIDs), calcineurin inhibitors, aminoglycosides, and osmotic agents before radiocontrast exposure. Regarding renin-angiotension-aldosterone system (RAAS) blockers, some studies note increased CIN risk whereas others show nephroprotection.
Does aminophylline reduce CIN?
Theophylline and aminophylline have the potential to reduce CIN through antagonizing adenosine-mediated vasoconstriction. These drugs have been tested in several small trials. Recent meta-analyses found that the mean increase in serum creatinine was significantly, but only slightly, lower at 48 hours after contrast among those receiving active therapy compared with placebo. The clinical importance of this finding is not clear. 36,37 There was heterogeneity among studies with regard to changes in serum creatinine. There is potential for adverse effects with theophylline. The optimal dose for prevention of CIN has not been established. Further studies are warranted.
What is contrast media?
Contrast media (CM) have low lipophilicity, low plasma protein binding, and minimal biotransformation. They quickly equilibrate across capillary membranes and have volumes of distribution equivalent to that of the extracellular fluid volume. In patients with normal renal function, CM are excreted with the first glomerular passage and the decrease in their plasma concentration follows a two-part exponential function: a distribution phase and an elimination phase.In patients with renal impairment, the renal clearance values are reduced. For example, 50% of the low-osmolarity contrast agent iomeprol is eliminated within 2 hours in healthy subjects, compared with 16-84 hours in patients with severe renal impairment.
How much water would be transferred by 100 ml of hyperosmolar contrast?
Rodby attempted to address these concerns, calculating that the administration of 100 mL of hyperosmolar contrast would move 265 mL of water from the intracellular to the extracellular compartment, resulting in an increase in extracellular volume by 365 mL. The increase in intravascular space would therefore be only a third, or 120 mL. Fluid shifts with low-osmolarity CM are even less. Rodby also found that extrarenal toxicity of CM was cited in mostly single case reports, and no objective evidence could be identified in three prospective studies. [ 53]
How many patients with CIN go on dialysis?
Fewer than 1% of patients with CIN ultimately go on to require dialysis, the number being slightly higher in patients with underlying renal impairment (3.1%) and in those undergoing primary percutaneous coronary intervention (PCI) for myocardial infarction (3%). However, in patients with diabetes and severe renal failure, the rate of dialysis can be as high as 12%. Patients who get dialyzed do considerably worse, with in-hospital mortality rates of 35.7% (compared with 7.1% in the nondialysis group) and a 2-year survival rate of only 19%.
How long does it take for CM to be removed from a hemodialysis?
High-flux dialysis membranes with blood flows of between 120-200 mL/min can remove almost 50% of iodinated CM within an hour and 80% in 4 hours. Even in patients with CKD, in whom contrast excretion is delayed, 70-80% of contrast can be removed by a 4-hour HD treatment.
Does sodium bicarbonate reduce CIN?
Furthermore, a meta-analysis and systematic review of 29 studies concluded that overall, hydration with sodium bicarbonate could significantly reduce CIN and the length of hospital stay compared with sodium chloride and that the addition of NAC as a supplement to sodium bicarbonate could increase prophylactic effects against nephropathy. In addition, hydration with sodium bicarbonate was found to be more effective in emergency coronary imaging and high-risk patients than in elective coronary imaging. [ 47]
Is no prophylaxis better than hydration?
The first study comparing no prophylaxis vs hydration, the phase 3 trial AMACING, found no prophylaxis to be non-inferior and cost-saving in preventing CIN compared with intravenous hydration. The AMACING trial included 600 high-risk patients with an estimated glomerular filtration rate (eGFR) of 30-59 mL/min/1.73 m 2) aged 18 years and older who were undergoing an elective procedure requiring iodinated contrast material administration. [ 37]
Can you take furosemide with matched hydration?
Diuretics on their own are not recommended but a recent meta-analysis suggested that furosemide with matched hydration by the RenalGuard System may reduce the incidence of contrast-induced acute kidney injury in high-risk patients undergoing percutaneous coronary intervention or transcatheter aortic valve replacement. [ 38]
Why do we need a physical exam for nephropathy?from ncbi.nlm.nih.gov
A physical examination is helpful in ruling out other possible causes of acute nephropathies, for instance, cholesterol emboli (pathognomonic findings of which are blue toes and livedo reticularis) or interstitial nephritis secondary to drugs (that typically involves a rash). There may be signs of volume depletion or there could be decompensated heart failure.
What is CIN in a nephropathy?from ncbi.nlm.nih.gov
Contrast-induced nephropathy (CIN) is a serious complication of angiographic procedures resulting from the administration of contrast media (CM). It is the third most common cause of hospital acquired acute renal injury and represents about 12% of the cases. CIN is defined as an elevation of serum creatinine (Scr) of more than 25% or ≥0.5 mg/dl (44 μmol/l) from baseline within 48 h. More sensitive markers of renal injury are desired, therefore, several biomarkers of tubular injury are under evaluation. Multiple risk factors may contribute to the development of CIN; these factors are divided into patient- and procedure-related factors. Treatment of CIN is mainly supportive, consisting mainly of careful fluid and electrolyte management, although dialysis may be required in some cases. The available treatment option makes prevention the corner stone of management. This article will review the recent evidence concerning CIN incidence, diagnosis, and prevention strategies as well as its treatment and prognostic implications.
How long does it take for renal impairment to return to baseline after contrast?from ncbi.nlm.nih.gov
A temporal link is thus implied. Post-contrast exposure, serum creatinine levels peak between two and five days and usually return to baseline in 14 days.
What is the third leading cause of iatrogenic acute kidney injury?from ncbi.nlm.nih.gov
Contrast-induced nephropathy is the third leading cause of iatrogenic acute kidney injury. The commonest cause is hypoperfusion of the kidneys causing either prerenal injury or acute tubular necrosis.[10] Moreover, the number and the type of risk factors directly affect the incidence of renal impairment. The incidence rate also depends on the procedure, with reports in the literature varying from 1.6-2.3% for diagnostic investigations to 14.5% overall in coronary intervention. [11]
What is CIN in contrast?from ncbi.nlm.nih.gov
Currently, the understanding of CIN is that it is the impairment of renal function gauged as either a 25% rise in serum creatinine from baseline or an increase of 0.5 mg/dL (44 µmol/L) in absolute serum creatinine value within 48-72 hours following intravenous contrast administration.[1]
Why is iodine used in cardiac procedures?from ncbi.nlm.nih.gov
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, diabetes mellitus, hypertension, and kidney failure due to contrast-induced nephropathy remains a growing concern. A sudden change in kidney function is a common complication of coronary angiography, and percutaneous coronary intervention, primarily because of contrast-induced acute kidney injury or contrast-induced nephropathy. This activity reviews the pathophysiology of contrast-induced nephropathy and highlights the role of the interprofessional team in its management and prevention.
Why is iodine used in contrast media?from pubmed.ncbi.nlm.nih.gov
Because of an increasing number of coronary angiography and coronary interventional procedures, the increasing use of contrast media, and the increasing number of invasive cardiac procedures being performed in high-risk patients with chronic kidney disease, ...
What is contrast induced nephropathy?
Contrast-induced nephropathy is most commonly defined as acute renal failure occurring within 48 hr of exposure to intravascular radiographic contrast material that is not attributable to other causes [ 3 ]. Ideally, the impairment of renal function should be measured by serial creatinine clearance, but because this step may be neither practical nor cost-effective in many centers, most of the literature describes the use of isolated measurements of serum creatinine levels, even though this parameter may be less sensitive at reflecting subtle early changes in renal function and may be slower to reach maximal sensitivity than creatinine clearance. Serum creatinine levels may prove to be more sensitive, however, in cases of preexisting renal impairment, in which tubular secretion of creatinine can lead to overestimation of the glomerular filtration rate (GFR).
Who reviewed contrast nephropathy?
Several authors have published in-depth review articles: most notably Katzberg [ 2 ], who performed a thorough review of urologic contrast agents and their potential effects, and Tublin et al. [ 1 ], who published a review in 1998 of current concepts relating to contrast nephropathy. Although many of their concepts still hold true, we intended to concentrate on risk-factor analysis and an updated and comprehensive review of current prophylactic agents, areas that, to date, have not, to our knowledge, been fully addressed while also providing a general overview of the issues relating to contrast-induced nephropathy that may be relevant to the modern radiologist.
How long after a contrast induced nephropathy should you monitor creatinine levels?
In patients at higher risk, renal function should be carefully monitored by measuring serum creatinine levels before and once daily for 5 days after the radio graphic procedure.
How to minimize nephropathy?
General measures to minimize the incidence of nephropathy include carefully considering whether the contrast examination is absolutely needed, especially in high-risk patients; using the minimal effective dose; and eliminating potentially nephrotoxic drugs (e.g., NSAIDs, aminoglycoside antibiotics, cisplatin, cyclosporin A, and amphotericin B) at least 24 hr before the study. The order of nil by mouth after midnight should be abolished in modern radiology departments in favor of protocols that allow clear liquids up to 2 hr before the procedure and that encourage IV hydration. Alternative diagnostic procedures should be considered in those at high-risk—for example, sonography and MRI. Interventional radiologists also have the option of using CO 2 angiography in high-risk patients, a luxury not afforded to cardiologists, neurointerventionalists, or those supervising CT studies.
Is diabetes a risk factor for contrast induced nephropathy?
Some authors have suggested that diabetes alone may be an independent risk factor for the development of contrast-induced nephropathy [ 9 ]. More recent research has failed to corroborate this connection. For example, Parfrey et al. [ 4 ], in a prospective trial of patients with diabetes, showed that none of 85 patients with diabetes and normal renal function developed clinically significant renal impairment (defined as an increase of > 50% in serum creatinine levels). However, given that those with diabetes alone were found to be at slightly higher risk of renal failure than the general population, it seems prudent to include diabetes in a preprocedural risk assessment.
Is osmolarity of contrast medium important?
Similarly, the osmolarity of the contrast media plays an important role with large clinical studies and meta-analyses indicating that the use of an LOCM substantially reduces the risk of nephropathy in high-risk patients compared with the use of HOCM (see section on Contrast Media under Preventative Treatments) [ 11, 16, 78 – 80 ]. However, this benefit could be shown only in patients with preexisting renal dysfunction in whom contrast material was administered intraarterially. In contrast, no benefit was found among those with normal renal function (with or without diabetes) in whom contrast material was given by IV [ 80 ]. A recent study suggests that iodixanol, a nonionic dimeric isoosmolar contrast medium (IOCM) with lower toxicity than LOCM, is of significant benefit in a group of patients known to be at high risk for the development of contrast-induced nephropathy [ 81 ]. However, further clinical trials are indicated to establish properly the role of contrast osmolality as a risk factor independent of the mode of administration.
Is calcium oxalate specific for contrast induced nephropathy?
Low urinary sodium and fractional excretion of sodium (< 1%) have been reported as being distinctive characteristics of this condition [ 2, 11 ], but these findings have not consistently been shown to be specific for contrast-induced nephropathy [ 12 ]. A persistent nephrogram on radiography or CT 24 hr after contrast administration is also said to be suggestive of a diagnosis of contrast-induced nephropathy [ 13, 14] but is not a consistent or a specific finding [ 8, 15 ].